ArticleJournal of bacteriology2012
Molecular basis of Yersinia enterocolitica temperature-dependent resistance to antimicrobial peptides.
Article in Journal of bacteriology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
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Who cites it
22 citing papers in PubMed, 40 citations in OpenAlex.
- Yersinia enterocolitica O:3 Outer Membrane Vesicles as a Platform for Complement Activation.Journal of extracellular vesicles · 2026Article
- Pathogenicity and virulence ofVirulence · 2024Review
- The Role of the Two-Component System PhoP/PhoQ in Intrinsic Resistance ofFrontiers in microbiology · 2022Article
- How the PhoP/PhoQ System Controls Virulence and MgMicrobiology and molecular biology reviews : MMBR · 2021Review
- Synthetic Phosphodiester-Linked 4-Amino-4-deoxy-l-arabinose Derivatives Demonstrate that ArnT is an Inverting Aminoarabinosyl Transferase.Chembiochem : a European journal of chemical biology · 2019Article
- Liberibacter crescens biofilm formation in vitro: establishment of a model system for pathogenic 'Candidatus Liberibacter spp.'Scientific reports · 2019Article
- Antibacterial activity of poly-l-arginine under different conditions.Iranian journal of microbiology · 2017Article
- LuxCDE-luxAB-based promoter reporter system to monitor the Yersinia enterocolitica O:3 gene expression in vivo.PloS one · 2017Article
- Bacterial Stress Responses during Host Infection.Cell host & microbe · 2016Review
- The RNA Chaperone Hfq Is Essential for Virulence and Modulates the Expression of Four Adhesins in Yersinia enterocolitica.Scientific reports · 2016Article
- Lipopolysaccharide Biosynthesis Genes of Yersinia pseudotuberculosis Promote Resistance to Antimicrobial Chemokines.PloS one · 2016Article
- Functional Genomic Screen Identifies Klebsiella pneumoniae Factors Implicated in Blocking Nuclear Factor κB (NF-κB) Signaling.The Journal of biological chemistry · 2015Article
- Regulatory principles governing Salmonella and Yersinia virulence.Frontiers in microbiology · 2015Review
- Host Antimicrobial Peptides in Bacterial Homeostasis and Pathogenesis of Disease.Antibiotics (Basel, Switzerland) · 2014Article
- Coinfection with an intestinal helminth impairs host innate immunity against Salmonella enterica serovar Typhimurium and exacerbates intestinal inflammation in mice.Infection and immunity · 2014Article
- Article
- Differential expression of two-component systems, pmrAB and phoPQ, with different growth phases of Klebsiella pneumoniae in the presence or absence of colistin.Current microbiology · 2014Article
- Thermal control of virulence factors in bacteria: a hot topic.Virulence · 2014Review
- Hexa-acylated lipid A is required for host inflammatory response to Neisseria gonorrhoeae in experimental gonorrhea.Infection and immunity · 2014Article
- The biology of the PmrA/PmrB two-component system: the major regulator of lipopolysaccharide modifications.Annual review of microbiology · 2013Review
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Antimicrobial peptides (APs) belong to the arsenal of weapons of the innate immune system against infections. In the case of gram-negative bacteria, APs interact with the anionic lipid A moiety of the lipopolysaccharide (LPS). In yersiniae most virulence factors are temperature regulated. Studies from our laboratory demonstrated that Yersinia enterocolitica is more susceptible to polymyxin B, a model AP, when grown at 37°C than at 22°C (J. A. Bengoechea, R. Díaz, and I. Moriyón, Infect. Immun. 64:4891-4899, 1996), and here we have extended this observation to other APs, not structurally related to polymyxin B. Mechanistically, we demonstrate that the lipid A modifications with aminoarabinose and palmitate are downregulated at 37°C and that they contribute to AP resistance together with the LPS O-polysaccharide. Bacterial loads of lipid A mutants in Peyer's patches, liver, and spleen of orogastrically infected mice were lower than those of the wild-type strain at 3 and 7 days postinfection. PhoPQ and PmrAB two-component systems govern the expression of the loci required to modify lipid A with aminoarabinose and palmitate, and their expressions are also temperature regulated. Our findings support the notion that the temperature-dependent regulation of loci controlling lipid A modifications could be explained by H-NS-dependent negative regulation alleviated by RovA. In turn, our data also demonstrate that PhoPQ and PmrAB regulate positively the expression of rovA, the effect of PhoPQ being more important. However, rovA expression reached wild-type levels in the phoPQ pmrAB mutant background, hence indicating the existence of an unknown regulatory network controlling rovA expression in this background.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.